Parenteral Provision of Micronutrients to Adult Patients: An Expert Consensus Paper

Plasma concentrations of several trace elements and vitamins decrease because of the systemic inflammatory response. Thus, low values do not necessarily indicate deficiency. The magnitude of this effect on plasma micronutrient concentrations was investigated to provide guidance on the interpretation of routine clinical results. Between 2001 and 2011, the results (2217 blood samples from 1303 patients) of routine micronutrient screens (plasma zinc, copper, selenium, and vitamins A, B-6, C, and E) and all vitamin D results (4327 blood samples from 3677 patients) were extracted from the laboratory database. C-reactive protein concentrations were measured as a marker of the severity of inflammation and categorized into 6 groups; for each group, plasma micronutrient concentrations and percentage changes were calculated. Except for copper and vitamin E, all plasma micronutrient concentrations decreased with increasing severities of the acute inflammatory response. For selenium and vitamins B-6 and C, this occurred with only slightly increased C-reactive protein concentrations of 5 to 10 mg/L. For each micronutrient, the change in plasma concentrations varied markedly from patient to patient. The magnitude of the effect was greatest for selenium and vitamins A, B-6, C, and D, for which the median plasma concentrations decreased by >40%. The clinical interpretation of plasma micronutrients can be made only with knowledge of the degree of inflammatory response. A reliable clinical interpretation can be made only if the C-reactive protein is <20 mg/L (plasma zinc), <10 mg/L (plasma selenium and vitamins A and D), or <5 mg/L (vitamins B-6 and C).

To confirm early, marked decrease in plasma selenium concentrations in patients admitted to a surgical and medical intensive care unit (ICU), and to study this decrease according to the presence or absence of systemic inflammatory response syndrome (SIRS), sepsis, or direct ischemia-reperfusion. Prospective, observational study. Collaboration between the adult ICU of a 1,100-bed general hospital and a biochemical research laboratory of a university medical center. One hundred thirty-four consecutive surgical and medical ICU patients. None. In the first 31 patients, plasma and urine selenium concentrations were measured by electrothermal atomic absorption spectrometry on admission and once weekly during their ICU stay. These values were compared first with severity scores, criteria for SIRS, sepsis, and organ system failure taken on admission, and then with nosocomial infection, organ system failure during ICU stay, and hospital mortality. An early, low mean plasma selenium concentration was observed in these patients compared with selenium laboratory reference values. Plasma selenium, measured on ICU admission, inversely correlated with Acute Physiology and Chronic Health Evaluation II or Simplified Acute Physiology II scores. Patients with SIRS had lower selenium concentrations than those without SIRS. Mean urine selenium losses were normal in the first 31 patients. Plasma selenium concentration was low in all patients with severe sepsis and septic shock (range 0.20 to 0.72 micromol/L) and in those patients with ischemia-reperfusion from aortic cross-clamping (range 0.34 to 0.68 micromol/L). Despite recommended specific selenium supplementation, plasma selenium concentrations remained low for >2 wks in patients with SIRS. However, there was a slight increase in plasma selenium concentrations in surviving SIRS patients, whereas plasma selenium concentrations decreased in nonsurviving patients. The frequency of ventilator-associated pneumonia, organ system failure, and mortality was three times higher in patients with low plasma selenium concentration at the time of admission (selenium < or =0.70 micromol/L) than for the other patients. In severely ill ICU patients with SIRS, we observed an early 40% decrease in plasma selenium concentrations, reaching values observed in deleterious nutritional selenium deficiency. This prolonged decrease in selenium concentrations could explain the three-fold increase in morbidity and mortality rates in these patients compared with other ICU patients. The efficacy of selenium treatment in SIRS patients with a high gravity index score or hypoperfusion needs further investigation.

The parenteral multivitamin preparations that are commercially available in the United States (U.S.) meet the requirements for most patients who receive parenteral nutrition (PN). However, a separate parenteral vitamin D preparation (cholecalciferol or ergocalciferol) should be made available for treatment of patients with vitamin D deficiency unresponsive to oral vitamin D supplementation. Carnitine is commercially available and should be routinely added to neonatal PN formulations. Choline should also be routinely added to adult and pediatric PN formulations; however, a commercially available parenteral product needs to be developed. The parenteral multi-trace element (TE) preparations that are commercially available in the U.S. require significant modifications. Single-entity trace element products can be used to meet individual patient needs when the multiple-element products are inappropriate (see Summary/A.S.P.E.N. Recommendations section for details of these proposed modifications).